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Smooth Muscle Group, Department of Physiology, The Queen's University of Belfast, Belfast BT9 7BL, Northern Ireland, United Kingdom
Isolated interstitial
("pacemaker") cells from rabbit urethra were examined using the
perforated-patch technique. Under voltage clamp at 
60 mV, these cells
fired large spontaneous transient inward currents (STICs), averaging
860 pA and >1 s in duration, which could account for urethral
pacemaker activity. Spontaneous transient outward currents (STOCs) were
also observed and fell into two categories, "fast" (<100 ms in
duration) and "slow" (>1 s in duration). The latter were coupled
to STICs, suggesting that they shared the same mechanism, while the
former occurred independently at faster rates. All of these currents
were abolished by cyclopiazonic acid, caffeine, or ryanodine,
suggesting that they were activated by Ca2+ release. When
D-myo-inositol 1,4,5-trisphosphate
(IP3)-sensitive stores were blocked with
2-aminoethoxydiphenyl borate, the STICs and slow STOCs were abolished,
but the fast STOCs remained. In contrast, the fast STOCs were more
nifedipine sensitive than the STICs or the slow STOCs. These results
suggest that while fast STOCs are mediated by a mechanism similar to
STOCs in smooth muscle, STICs and slow STOCs are driven by
IP3. These results support the hypothesis that pacemaker
activity in the urethra is driven by the IP3-sensitive store.
D-myo-inositol 1,4,5-trisphosphate; spontaneous transient inward currents; spontaneous transient outward currents
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